Abstract
Circadian rhythms are generated by the cyclic transcription, translation, and degradation of clock gene products, including
(
), but how the circadian clock senses and adapts to temperature changes is not completely understood. Here, we show that temperature dramatically changes the splicing pattern of
in
. We found that at 18°C, TIM levels are low because of the induction of two cold-specific isoforms:
and
. At 29°C, another isoform,
, is upregulated. Isoform switching regulates the levels and activity of TIM as each isoform has a specific function. We found that
encodes a protein that rescues the behavioral defects of
mutants, and that flies in which
is abrogated have abnormal locomotor activity. In addition, miRNA-mediated control limits the expression of some of these isoforms. Finally, data that we obtained using minigenes suggest that
alternative splicing might act as a thermometer for the circadian clock.